Zebra reverse-availability bias (noun):

The observation that reading about a rare condition is quickly followed by a patient encounter with the same condition.

If you read about it, they will come...

Don't forget to check out the other glossary entries!

@justanerdoc airway mgt or trauma resus, you pick.

— Klint W. Kloepping (@KlintWKloepping) April 20, 2013

There he is.

I've been trying to find this paper for a while, finally was able to. I saw Judd Hollander quote it in a grand rounds as PGY2:

Costochondritis. A prospective analysis in an emergency department setting.


This might be the coolest chest pain study ever done.

Rheumatologists evaluated 122 consecutive ED patients with chest pain at the Cabrini ED in 1991-2, and used the American College of Rheumatology criteria for diagnosing costochondritis.

Costochondritis was identified by digital palpation, applying enough pressure to induce partial blanching of the examining finger (=4 kg/cm2), over the costochondral and costostemaljoints (CCSJ), as previously reported. Patients were asked if such a maneuver: (1) caused no pain, (2) caused a pain different from original chest pain, or (3) caused a pain similar to the original one. Patients were considered to have CC if the answer was (2) or (3). The rest was used as a control group. Not included in this study were patients whose chest pain was associated with recent trauma, surgery, infection, fever, or malignancy.

Punchline:
6% of patients with costochondritis diagnosed by Rheumatologists in the ED = acute MI.

That's right. One out of every 17 patients who was diagnosed by a Rheumatologist, using the ACR costochondritis diagnostic criteria were having a heart attack.

Not ACS. Not positive stress. Biomarker-positive my-o-cardial in-farct.*

Judd Hollander's conclusion was: don't ever use the word costochondritis. If a resident uses it, send them home for the day because they did a bad job.

One big question remains:

How hard were these Rheumatologists pushing?**

For features from the HPI that make ACS more likely, see Salim Rezaie's great summary in Academic Life in EM.

A great question came up:

@mdaware @mgkatz036 Who has ever seen a Rheum in an ED, and why were they seeing CP pts?
— Cynic (@Apathetic_Cynic) March 29, 2013

(Perhaps that's why Cabrini closed?)

On a historical note, I find it interesting that the authors included this line in their discussion:

One of the most interesting observations in  this study was the low frequency ofAMI in the CC group,  which was four times lower than in the control group, in spite of having similar risk factors for CAD,  based on age, history of smoking, and hypertension.

*plasma CK-MB. It was the early 1990s. 

**Actually we know: about 4 kg/cm2, "enough pressure to induce partial blanching of the examining finger"

This question has come up a few times, so I figured I'd put it down in one place:

Breast pocket:
2 pens
Sharpie (industrial) for marking landmarks (#13; eg cric, LP, and paracentesis)
scalpel
Rear pocket:
2 sheets of paper, folded in quarters for signout, notes, etc.
iPhone (not pictured, because it's taking the picture)

Waistband:
Trauma shears: most useful ED tool


ID:
mini-LED (cheap ones; example)
retractable reel clip
Desk:
stethoscope. still useful in a handful of situations, mostly wheezing, reiki, and leading into questions about smoking.
Shift bag:
head lamp (AA battery powered) for things like finger & scalp lacs
big clamp
meconium aspirator & swivel adaptor for messy airways
extra guaiac cards & developer
3-way stop cocks -- poorly stocked in my ED, can come in handy (here, here, here, here, here, here)

crackophenia (noun):

The patient has crackophenia hair.

The patient has neck & face tattoos

With all due respect to Darren Braude (who is both smarter and significantly more qualified than me!) I'm admittedly not a huge fan of RSA -- rapid sequence airway. The concept is simple: give RSI meds (sedative + paralytic), place EGA* to preoxygenate, then intubate. The main concern I have is that you are taking patients who already think there might be an issue in oxygenating, and paralyzing them. Not much of a safety net.

However, the main reason I don't like RSA isn't because RSA is terrible or wrong but because the patients who need RSA are sick, tricky patients and all paths are fraught with danger.

There's been an twitter discussion over the past day or so between Nicholas Chrimes, Minh Le Cong, myself, and few others (Pik Mukherji, Alexander Sammel, Taylor, Brent May, Alan Grayson, Crystal Upshaw, Chris Edwards, Valerio Pisano, Kath Woolfield... sorry if I missed anyone!). And sometimes 140 characters (plus all the @tags taking up space) just isn't enough.

The main discussion skeptic of RSA here is Nicholas Chrimes, who asks:

Why not just try to intubate these patients? If they desat or the airway is unexpectedly difficult, then place an EGA and reoxygenate.

To me, the patient who needs RSA is the patient who you need to intubate now (no time for awake or AFOI or OR), and while you can preoxygenate, that preoxygenation is tenuous. This is admittedly a very, very small group of patients (smaller than the small group of patients who require DSI).

And I want to be very specific: I mean the patient who is preoxygenated to 100% on NIV for 3 minutes with 10 of PEEP and by the time the spatula hits the glossus, the sat is 85%. Doesn't happen much but when it does, no one is happy.

I think that the best thing you can do with this patient is slip in an LMA, reoxygenate, then intubate via the LMA. Dr. Chrimes disagrees, for a few reasons.

First, he contends that an attempt at ETI is just as fast as LMA placement. I disagree. I think that in the time it takes me to get the blade in the mouth, I could already have the LMA in place and start reoxygenating. I haven't done a formal lit search on this but in addition to my experience, there is at least one paper that at least suggests it (PMID 22796543**).

Next, Dr. Chrimes suggests that the goal is airway protection from aspiration, not oxygenation. Aspiration is very bad, but I think one of the lessons from NAP4 is that desaturation kills in the ED, aspiration kills in the OR.

As Minh suggests, in these patients the risk of aspiration is low but the risk of critical desaturation is very real and the consequences are dire. The goal here isn't to leave an LMA in place. It's to get the patient to a protected airway without critically desaturating. The patient who critically desaturates injures their brain and/or arrests. Which is bad.

“It's not about plastic in the trachea, it's about oxygen in the lungs." (Rich Levitan)

I don't think the answer is necessarily clear. But to me, this seems like the least dangerous path in a very dangerous patient.

*Extra glottic airway, such as a laryngeal mask or King-LT. I happen to prefer LMAs -- and I know that technically LMA is a brand name but I don't want to keep typing "laryngeal mask"

**I happen to have been a subject in this study

Kudos to ACEP for joining the Choosing Wisely campaign! I think this is a big step forward in helping reign in unnecessary care, which not only will help our patients but also happens to save money. Note that helping patients is the priority here; saving money is nice added benefit (and will help keep other people's noses out of our professional business).

As explained briefly on The Central Line:

“Choosing Wisely” is part of a multi-year effort of the American Board of Internal Medicine (ABIM) Foundation to help physicians be better stewards of finite health care resources. The campaign encourages medical specialty organizations to identify five tests or procedures commonly used in their field, the necessity of which should be questioned and discussed by patients and physicians.

ACEP had considered joining 3 times before, but was concerned that and most recently had declined to join in the summer of 2012. Some concerns expressed by then-ACEP president David Seaberg include:

Many of these patients have been sent in with expressed instructions from the family physician to have this or that test ordered 

It is simply not possible for emergency physicians to talk about reducing ‘unnecessary’ testing without including messages about the need for medical liability reform.

it very well may assure that emergency physicians will not receive reimbursement for the five identified procedures or tests.

Although those concerns are not unwarranted (mostly the latter 2), I think they are generally outweighed by the benefits. As I explained in a reply on the EP Monthly re-post of the same essay by Dr. Seaberg:

Choosing Wisely is gaining national recognition for its patient-centered approach to decreasing unnecessary care. This is one major way we -- as professionals -- can decide what is appropriate for our patients. Parsimony is coming. If we don't take the lead then others will decide how we should care for our patients. As a specialty, we can define our standard of care so groups like CMS don't have to.

Patient says he is short of breath, I asked when it started and I'm told "any minute now." Me: so you are not short of breath now? Pt: "no"
— HopHeadMD (@HopHeadMD) February 18, 2013

Colleague has a pt w CC: chest pain that started while driving to the ED. Prescient, that patient.
— GruntDoc (@gruntdoc) February 18, 2013

note that:
a) these were 2 minutes apart
&
b) these guys do not work together

Seldinger's Cat or Schrodinger's Wire (noun):
when you just don't know which vessel the wire is in...

Don't forget to check out the other glossary entries!

True story: a few months ago, I walked into my apartment, and noticed the sink was overflowing with dishes. My first reaction: The dishwasher must be full.

I had been taught a few years ago that the main cause of crowding in the ED is boarding of admitted patients: patients who came to the ED, got admitted, and are waiting for beds upstairs. It seemed a bit odd at first, but the explanation makes sense. There are 3 possible causes: input, throughput, and output. Either there are too many patients coming to the ED; patient time in the ED is too long; or, we can't get patients out of the ED.

While the mainstream media and many policy people who aren't fluent with the topic are quick to attribute crowding to armies of low-acuity patients clogging up EDs with sore throats and ankle sprains, empirical evidence shows that's just not the case.

And it makes sense. If an admitted patient sits in the ED for an extra 6 hours, that's the equivalent load as 6 low-acuity patients who each take an hour. They may not take up a lot of physician time (although they do use some) they require a nurse, and a space in a room (or hallway).

Same idea with throughput. Although some emerging evidence suggests that throughput is a bigger factor than we thought. But much of this is probably due to EDs doing more comprehensive workups in order to avoid admitting patients.

So why is boarding such a pervasive problem? The reasoning is that hospital administrators think that hospitals generate more revenue from elective, procedural admissions than from ED admits. Therefore, elective surgical schedules are kept full in order to bring as as much revenue as possible, and the ED patients will still get admitted (after waiting for a while). If hospitals cancelled elective admissions because the hospital was full, they would forgo that revenue.

However, there is some evidence that this calculation is mistaken, and hospitals actually lose revenue by filling up the hospital, forcing the ED to go on diversion, so that critically ill patients are lost (and they pay pretty well).

Oh, and keeping the ED crowded leads to all sorts of badness for the patients, not just longer wait times but worse care.

Further, lack of space in rehab and nursing facilities (and lack of payment by insurers) is another hospital-output problem, particularly for public hospitals.

In addition to dialing down elective procedures, hospitals can help with crowding in a number of ways. Overall, a lot of it is a matter of hospital operations (the business/admin stuff, not the surgical stuff. coincidence?) Simple things like automatically calling housekeeping to clean a room when an inpatient is discharged.

Perhaps the best plan, concocted by Peter Viccellio, is brilliantly simple. If all the admitted patients can wait in the ED hallways, why can't we spread them throughout the inpatient hallways? There are certainly a lot of hallways and nurses upstairs, too. It's been shown to be safe, preferred by patients, and, not surprisingly, places that institute inpatient hallway boarding "magically" find beds for half of the hallway boarders fairly quickly.

Yet EDs across the nation are still crowded, most of the time, pretty much everywhere. Perhaps if hospitals made better decisions, things would be better -- for revenue, for healthcare workers, and for patients.

@mdaware if there wasn’t ROSC, it’d be a preflordial crump.

— Michael Katz (@MGKatz036) January 16, 2013

Don't forget to check out the other glossary entries!

Ditto MT @precordialthump: @mdaware If u think s'thing is crap, leave a comment, tweet it, or write yr own blog... Ditto if its good #FOAMed

— Javier Benítez (@jvrbntz) January 18, 2013

@mdaware @jvrbntz @precordialthump It was actually your second post.Glad that I could stimulate you to blog and tweet!

— Robert Centor (@medrants) January 18, 2013

Here's my SMACC PK on Capnography

“Airway day? Every day is airway day!”

- Minh Le Cong

Minh gets himself a CL-1 on... himself

In addition to the countless posts and presumably a real job, Minh Le Cong has been putting together a free online airway curriculum. So far he has 4 episodes, here's what we have so far:

#FOAMEd Online Airway training Program – Anatomy review lecture by Dr Seth Trueger
we discuss airway anatomy

#FOAMEd Online Airway training Program – POSITIONING AND BLADE USE with Trueger and Faust
we talk about positioning and some techniques for laryngoscopy
featuring special guest and magnesium enthusiast Jeremy Faust

#FOAMEd Online Airway training Program – more Anatomy, blade technique and topicalisation by Dr Seth Trueger
Featuring a guest appearance by Minh's glottis

PHARM Podcast 52 : #FOAMEd Online Airway training Program – Airway Decision making
Featuring one of my airway mentors, the incomparable Reuben Strayer, and a tough case from Alexei Wagner

Congratulations to Brendan Carr & Robert Welch for the first MDaware Outstanding Reference Award for #6 in Traumatic Intracranial Hemorrhage, Value in Health Care, and Being Important (currently e-pubbed).

The article is a very nice piece on patient-centered care and evidence for GCS-15 ICH patients and is worth a read.

The ORA is given here for:

• appears in a legitimate publication
• quotes a fictional character
• cites of Wikipedia
• excellence of reference
• Bonus Points awarded for referencing the Will Rogers Phenomenon.

@thewellnesslife 6-8ml/kg IBW;16-18/min titrate to PaCO2; 100%/PEEP5 titrate to SpO2 via ARDSNet; RAD? low PEEP slow rate, hiCO2 okay! *BAM*
— Seth Trueger (@MDaware) November 29, 2012 

Don't forget to check out the other glossary entries!

from Steve Carroll (@embasic):

rocuropenia - noun

In need of endotracheal intubation, and, more to the point, paralysis.

That trauma patient was being rowdy with signs of rocuropenia...

Related:
   benzopenia
   hypoplastic vocal cord syndrome

The treatment for heartburn these days is antiplatelets, serial troponins, a negative stress test and then antacids.
— Chump (@bungeechump) November 1, 2012

@mdaware @realeddoc Absolutely. Nitro by ambulance and a misplaced prehospital ECG. Bad combo.
— Chump (@bungeechump) November 1, 2012

From EM Clinics of North America:

Relieving factors

Many individuals incorrectly assume that because a patient's chest pain is relieved with nitroglycerine, the pain is more likely to be cardiac in nature. In examining this question, Henrikson and colleagues [39] found a higher incidence of relief of chest pain in patients without ACS than those with active ischemia. Steele and colleagues [40] also found that nitroglycerine relieved chest pain in 66% of patients who were ultimately diagnosed with noncardiac chest pain. This data shows that chest-pain relief by nitroglycerine had no value in predicting or disproving ACS. Similarly, physicians have used the GI cocktail (a mixture of antacids and viscous lidocaine) to prove the likelihood of a GI cause and disprove the presence of ACS. There is no recent literature supporting the use of the GI cocktail for differentiating these types of pain, but the practice persists. Many physicians believe that burning substernal pain relieved by antacids is clearly caused by esophagitis or gastritis. Subsequent studies have actually shown that “burning” chest pain or pain described as “indigestion” may be as strong a descriptor of ischemia as chest pressure. [28],[31] In a small descriptive study, Wrenn and colleagues [41] found indiscriminate use of the GI cocktail for various ED complaints. In this subset, a significant portion of patients who were subsequently admitted with possible myocardial ischemia reported total or partial relief after administration of a GI cocktail.

In summary, chest-pain relief with either nitroglycerine or GI cocktail does nothing to improve the diagnostic accuracy for ACS and should not be used to influence decision making. (emphasis mine)

Relief of symptoms with nitroglycerin is not helpful in distinguishing ACS from GERD. Unfortunately, most ED patients with GERD-like symptoms therefore also have anginal-like symptoms, and most will need an ACS workup. It's not that the ACS workup relieves GERD symptoms; rather, in the ED we don't diagnosis patients. We "risk-stratify" (particularly with potential ACS) and determine which life-threatening diagnoses are potentially present, and whether the chance of that life threat is worth is sufficient to warrant workup (or treatment).

So in a sense, yes, the ED treatment for heartburn is an ACS workup.

But maybe someday without a stress test.


[39]  Henrikson C.A., Howell E.E., Bush D.E., et al: Chest pain relief by nitroglycerin does not predict active coronary artery disease. Ann Intern Med 139. (12): 979-986. 2003.

[40]  Steele R., McNaughton T., McConahy M., et al: Chest pain in emergency department patients: if the pain is relieved by nitroglycerin, is it more likely to be cardiac chest pain? CJEM 8. (3): 164-169. 2006.

[28] Goodacre S.W., Angelini K., Arnold J., et al: Clinical predictors of acute coronary syndromes in patients with undifferentiated chest pain. QJM 96. (12): 893-898. 2003.

[31] Lee T.H., Cook E.F., Weisberg M., et al: Acute chest pain in the emergency room. Identification and examination of low-risk patients. Arch Intern Med 145. (1): 65-69. 1985.

[41]  Wrenn K., Slovis C.M., Gongaware J.: Using the “GI cocktail”: a descriptive study. Ann Emerg Med 26. (6): 687-690. 1995.

Warning: this may sound crazy at first. But hear me out, listen to my anecdotal evidence* and then try it out for yourself.

Nurses are excellent at placing peripheral IVs. Occasionally, some patients are too tough and the nurses turn to us. Not because we're any better -- they place plenty more IVs than we do -- but because we can use sites they aren't allowed to (EJ), perform invasive procedures (CVC & IO), and have tools they usually aren't allowed to use (ultrasound -- great video from the US guys!). These are all methods that work, but take time, and sometimes the US-guided peripheral just won't take.

Sometimes the nurses get the line (hurray!) but couldn't get the labs (oh no!) -- which is frustrating (or at least, it used to be). The recourse I see a lot of people take is the arterial stick, invariably a blind radial draw. Seems reasonable -- you can feel the pulse, it only takes a few minutes, and is successful ~80% of the time.** If you're savvy at US then it's even more likely to be successful. But I have seen many a tiny and/or squirrelly radial artery, and those do not like being poked.

Here is my fail-proof method:

Ultrasound-Guided Femoral Stick

This may sound drastic. I used to reserve it for sick patients -- those critically ill enough to have pharmacologic or endogenous sedation, or at least those who seemed sick enough to warrant it. But mission creep set in, and now I will do it on nearly anyone who needs blood drawn but not a catheter.

This may seem extreme, particularly when the radial is an option. But in my head, this takes a 5 minute procedure with an 80% chance of success into a 30 second procedure with a 100% chance of success. In the words of Dogbert, it's like sandblasting a soup cracker.

I tell the patient that it may sound crazy, but that I really think this will be better than digging around in their arm for 5 minutes -- which they invariably just went through about 3-10 times before the nurse called me over.

Of course this is anecdotal, but when I ask (awake) patients if this was better or worse than a other sticks (i.e. peripheral IV placement or blood draw) they invariably say the groin was MUCH less painful. There was one even one awake guy with a fully functioning brain and nervous system where we had a conversation through the entire fem draw, and he didn't feel a thing. Nothing! He didn't believe I had even poked him until I showed him the 20 mL syringe full of his blood.

I've started telling patients that while it may seem scary and will hurt a bit because, well, it's still a needle, but that enough patients have told me it's better than the arm pokes that I feel comfortable telling them it's less painful than any other option. And afterward, every awake patient has agreed.

The simple steps:

GEAR:

• 18g needle
• 20-30 mL syringe (smaller if you only need 1 lab)
• US with vascular probe
• alcohol or chloroprep
• gauze & tape
• lab tubes (& ice if getting lactate or BG)
• 3-way stopcock
• vacutainer
• lab labels

*Similarly, Aaron Johnston spoke about procedural sedation for manual disimpaction on Rob Orman's ERCAST. Sounds crazy at first, but once you see it, everyone is convinced. Level of evidence: A for Anecdotal

**Level of evidence: M for Made up number

Image: Peter Cushing as Dracula. Before blowing up Alderaan as Grand Moff Tarkin, he was a B-movie vampire. "Don't make your patient a pin-cushion -- Peter Cushing"

Gave a talk on heterotopic today.Orthopedist keep scratching his head and said, “That just ain’t right. Are you sure that’s possible?”
— a midwest er doc (@docERtrauma) October 25, 2012

One of the ideas thrown around to save Medicare costs is to increase the age of eligibility from 65 to 67 (Social Security is undergoing a slow transition from 65 to 67, initiated by Congress in 1983). It seems to make sense: people live & work longer, so let's adapt and save some money.

But it looks like it wouldn't help very much.

These numbers below are from a 2011 analysis by the Kaiser Family Foundation I recently reviewed for journal club. For more (but not too much) detail, there's a great Executive Summary on page 5.

If the age change suddenly went into effect in 2014, this is what would happen in the first year:

• Federal savings: 
• $5.7 billion (1% of total Medicare costs)
• Increased costs:
• 65-66 year olds: $3.7 billion
• Employers: $4.5 billion
• States: $0.7 billion (via Medicaid)
• Premiums: 3% increase for both Medicare recipients and those insured through the Health Insurance Exchanges

A bit more detail:

• 5 million enrollees would be affected (there are roughly 50 million now, 42 million >65 years old and 8 million <65 but disabled)
• Medicare would decrease spending by $31 billion but the total federal savings would only be $5.7 (about 1% of Medicare spending) billion due to increased costs in Medicaid, subsidies through the exchanges, and decreased revenue from Medicare premiums
• Out-of-pocket costs for 65-66 year olds would rise $3.7 billion
• Employers would spend an extra $4.5 billion
• Premiums would increase for 2/3 of 65-66 year olds (about $2200/year each)
• Premiums would decrease for 1/3 of them, largely through subsidies through the exchanges
• 42% of 65-66 year olds would receive insurance through employers
• half would still be working
• half through a spouse or through a retiree plan
• 38% would get insurance through the exchanges
• 20% would get insurance through Medicaid
• Premiums in Medicare and the exchanges would both increase about 3%
• Will Rogers phenomenon: the healthiest seniors would leave Medicare, making both the Medicare pool and the non-Medicare pool sicker on average

I'm a big fan of rocuronium for RSI. The argument is succinctly -- and arguably definitively -- made by Reuben Strayer in 8 minutes.

One of the cornerstones of the argument is the landmark paper by the Benumof Brothers*: patients will invariably desaturate before the sux wears off.

The ubiquitous "time to hemoglobin desaturation curve" that is shown in every airway talk, chapter, paper, etc:

Benumof JL, Dagg R, Benumof R. Critical hemoglobin desaturation will occur before return to an unparalyzed state following 1 mg/kg intravenous succinylcholine. Anesthesiology. 1997 Oct;87(4):979-82.

...not only comes from this paper, but was specifically made to demonstrate that the patient will desaturate before the sux wears off.

But wait a minute. This is from 1997. This was before NODESAT -- the use of nasal cannula during laryngoscopy to maintain oxygen saturation.

Does nasal oxygenation during laryngoscopy bring succinylcholine's shorter duration of action back into the question?

My thoughts are below this other mandatory airway management picture:


My answer is no: roc still beats sux.

• Sux risks hyperkalemia, i.e. succinylkalemia
• When the sux wears off, the patient won't be breathing calmly cleanly. They will be fighting like heck because people are stabbing them in the back of the throat
• The patient who can't get intubated in 8 minutes still needs to be intubated (there is no "cancel case" in the ED) -- and more paralyis is helpful for bagging, placing an LMA, cric, etc.
• Intubating conditions are as rapid and as good with roc
• Sux may lead to faster desaturation, because even with NODESAT...
• NODESAT is amazing but not 100% perfect:

*There are 2 Benumof authors on the paper -- Jonathan and Reuben. I don't know for certain but I like to think they are brothers, and I think they should play the Brugada Brothers in a game of basketball.

**Level of Evidence: A for Anecdote

from Casey Parker:

lung lint - noun

The small, subsegmental PE you wish you had not diagnosed as it almost certainly clinically irrelevant.

hypoCTemia - noun

The state or condition of urgently needing a CT scan, possibly due to low levels of endogenous CT.

I got in a recent twitter discussion with a number of people -- mostly @movinmeat -- on the impact of low acuity patients in the ED. He responded with an excellent, well-reasoned, but probably incorrect blog post. This is largely a response to both that conversation (edited Storify version here) and his excellent post. He asks: are low acuity patients congesting the ED? And his answer is yes. But I disagree. And it's fun to argue with people who you generally agree with.

Nobody likes the low acuity patients who come to the ED. Few of us went into EM to take care of not-so-sick patients, there's a lot of charting, and there are just so many of them, which is why for years everyone thought that they were cause of crowding in the ED. But they're not. It's been studied very well, and the overwhelming cause of ED crowding is the boarding of admitted inpatients. ACEP has a report about it. There's even a big IOM report about it. Low acuity patients are frustrating, but not the problem.

When it comes to crowding, are low acuity patients just a drop in the bucket?*

The basic model is input/throughput/output. There are so many patients who come to the ED (input), they take so much time in the ED getting histories, IVs, xrays, etc (throughput) and then they eventually leave (output). The patient with the cold takes, say, an hour. The patient getting serial troponins for chest pain takes 6 hours. The patient admitted for an appy takes 4 hours... PLUS whatever time he sits around waiting for a bed upstairs (boarding). It's easy to see why 1 admitted patient waiting around for an upstairs bed takes up a much bigger piece of the pie than the silly URIs.

(One bit of background: there's some decent work that shows that time in the ED is a great estimate for overall resource use in the ED -- patients who are there longer take up nursing time, ask the doctors questions, use more tests, take up a spot, etc.)

Next, consider what clogging the system really means.

We are quick to think about low-acuity ED visits as "unnecessary visits" -- like the healthy patient with a cold. Isn't the admitted patient boarding in the ED in the ED unnecessarily?

Here's a simple example: a patient comes in with a twisted ankle. We do 2 main things: make sure this was a mechanical fall (history) and apply the Ottawa rules (physical), which is negative (assessment) and we tell the patient that they don't need an xray (plan). Rx 800mg ibuprofen, send home with return instructions. Explain again that they don't need an xray. Realistically, this takes an hour from door to door (although it probably shouldn't).

Now a 50 year old with diabetes and CAD comes in with chest pain, with some concerning T-wave changes. Took his aspirin just before he got here. Is otherwise rock-stable. Slam dunk admission. Write some notes & orders, talk to the hospitalist. Done in 10 minutes. Now they just need to go to that inpatient bed. What happens if they board for an hour? or 4? or 12 hours?

When I was in residency we would routinely board 30 patients at least 6 hours each every weekday. That's 180 patient-hours. As MM notes, the total facility time is a great estimate for resource load.

So even if we are pessimists and assume every ankle and URI takes an hour, that's still 180 URIs we could have seen.

Here's a graph that MM posted showing distribution of ED patients by LOS and disposition:


Lots of discharged patients are in the ED for a few hours. But I think this graph is misleading with respect to how much time they spent in the ED.

I reran his same numbers (being as true as possible from these graphs). I broke this up into 3 groups: discharged in 2 hours or less, discharged but LOS 2.5 hours or more, and admitted.

One major caveat: with these data, anyone who stayed 6 hours or later is counted only counts for 6 hours. That is, my numbers underestimate the burden of the patients with high LOS (which is 1/3 of the admitted patients)

How many patients were there in each group?

DC 0-2h: 41%
DC 2.5-6h: 39%
Admit: 20%

How was LOS divided among these patients?

DC 0-2h: 20%
DC 2.5-6h: 45%
Admit: 35%


That is, 40% of the patients are discharged in 2h or less, but only take up 20% of the hours. The 20% of patients who got admitted take up 35% of the LOS, and again, that underestimates their share because it treats everyone over 6 hours as taking only 6 hours. And, this is assuming that everyone who is discharged in 2 hours or less is a low-acuity patient.

So maybe not a drop, and maybe more than a spoon. But the quick discharges are taking only a small portion of the total resources. And remember, this is only 1 hospital, and it's a hospital with remarkably little boarding.

But even further: is that even the right group of patients to consider as "low acuity" or "shouldn't be in the ED"?

It's very tough to properly measure the low-acuity patients.

I agree that the 8% figure frequently quoted by ACEP is misleading. Not only is it based merely on triage category, which as @movinmeat notes may be incredibly misleading, but those recommended to-be-seen times are entirely made up. And it's very hard to figure this out based on administrative data.

These are all patients that we frequently see and discharge with neck pain:

• mild fender bender
• serious MVC
• 30th visit for chronic neck pain (gabapentin refill)
• 80 year old who was worked up (appropriate or not) for a cervical artery dissection

Is discharge from the ED a sign that the visit was unnecessary? Of course not. How many patients get seen for potentially worrisome chief complaints and end up being discharged home? (Hence the prudent layperson standard.)

About 80-85% of all ED visits get discharged. Were these all visits that didn't need to be seen in the ED? What are the alternatives? Primary care offices? Urgent care center? Walgreen's? How easy is it to get into any of those? What are the hours? Most PMD offices are open during business hours, which is when many of us are actually at work. If you twist your ankle and don't know if it's broken, is it inefficient to come to the ED, where the lights are already on, the x-ray machine is running, and the tech is there?

I don't enjoy the low-acuity patients. They're not that interesting, they make the haystack bigger (when a big part of our job is looking for needles), they talk back more, and if I wanted to work in an outpatient clinic I work in an outpatient clinic.

But low acuity patients:

• don't cause crowding
• don't have a lot of alternatives
• and, as ACEP President David Seaberg notes, make us money

*I had modified that to a spoon in the bucket

Low risk chest pain (or any of its analogues) is one of the most common chief complaints in the Emergency Department (I think it's #2?) yet there is a huge amount of practice variability (more on this at the end), discrepant teaching, and huge unanswered questions.

Recently, the European Society of Cardiologists determined that unstable angina is no longer a thing, much like hypertensive urgency, the American auto worker, travel agents, and rock saxophonists. The ESC concluded that high-sensitivity troponin (hsTn) is sensitive enough to rule out ALL acute coronary syndrom (ACS).

If hs troponins are completely neutral in a patient with chest pain, it's impossible that the patient has significant coronary disease. (Freek Verheugt, Dutch cardiologist)

I hope he's right. But I don't think he is. I of course respect cardiologists, the European Society of Cardiologists, and recognize that I am but a junior emergentologist (and resuscitationist). And, I would love for it to be true. If we had an accurate biomarker for ACS, we could admit fewer patients, do fewer unnecessary stress tests and caths, and offload a lot of potentially unnecessary hospital admissions, decompressing some nontrivial level of ED & hospital crowding.

I humbly submit my dissent based primarily on the fact that there are plenty of simple questions left open by the data on hsTn. I am also intentionally not putting robust references in this post precisely because I think there are more questions than answers -- enough that I want readers to have to go to the literature to draw their own conclusions.*

First, some simple background.
The spectrum of acute CAD:

• none
• stable angina / baseline CAD: established over time with a PCP or cardiologist.
• unstable angina: diagnosed based on H&P, ECG, and (arguably) with stress, CTCA, cath, or observation (e.g. autopsy)
• NSTEMI: diagnosed by cardiac enzymes
• STEMI: diagnosed by ECG

I think there is a subset of chest pain patients who are hsTn negative, but still have ACS/UA, and are therefore at increased risk for MI or death in the short term.

What to do with them? Stress test may not help; CTCA is probably just another stress test. And PCI during UA probably doesn't help most patients. (except maybe for patients with Wellens syndrome?)

So now what? That means we have patients who have chest pain, aren't having MIs, and might be having UA. Stressing or cathing them probably doesn't add much, but they are still at risk. Is admission the answer? The benefits of admission are essentially monitoring (if your UA progresses to NSTEMI or STEMI it will hopefully be caught in-house), medication optimization (ensured you're put on aspirin, BP managed, etc), scared straight (tobacco cessation?).

Again, I'm not sure what to do with all of this. But back to widely divergent practice patterns:

I recently spoke with a friend who was a year ahead of me in residency. At his hospital group, if you have 2 negative troponins (not high-sensitive) and a normal ECG, you go home. At the same time, a malpractice insurer for a hospital network in the same geographic area told all their ED docs to admit every chest pain because too many cases of ACS were being missed. So the standard of care is somewhere between doing nothing and everything.


*EMCrit explained this tactic at one point, can't find it now. Obviously it's not good to do all the time and can be abused to cover laziness, but there's such divergent information on chest pain that I think it applies here.

I've been kicking around my thoughts on low risk chest pain for a few years now. Special thanks to Manrique Umana for pushing me over the edge.
Also thanks to Nick Genes, Ryan Radecki, Dave Newman, Luke Hermann, and Richard Body for being the main influences to my gestalt & interpretation of the evidence on this.

This is adapted from an email I sent to Minh Le Cong.

Haney Mallemat recently hosted a number of us what will hopefully be the first in a long series of international EMCC real-time discussions, with participants including Haney, Scott Weingart, Rob Bryant, Jeremy Faust, Steve Caroll, myself, Laleh Gharahbaghian, and of course, the ubiquitous Minh Le Cong. (video of the discussion should hopefully be up at some point)

Two related topics came up:

1. Is DL dead? 
2. Is ultrasound necessary for IJ & femoral lines?

It is not lost on me that these are very similar questions, and I come down on different sides with each.* I want to explain why I see 2 very similar situations and come to 2 different conclusions.

With respect to ultrasound for IJ & femoral lines, I think that it is clear that the landmarks are simply not reliable. I don't have hard references (although people who taught me assure me they exist) but the Sinai US guru Bret Nelson loves to take junior residents, show them the nice "NAVEL" shot and then scan up and down and show how the anatomy changes -- the relationship between the femoral artery and vein is much more complex, variable, and dangerous. I have done this on nearly every femoral line I have done** and it is shocking. Similarly, Scott Weingart has shown data on the IJ similarly just not being reliably related to the carotid.

I think Marik is possibly (probably?) correct and in the era of monitoring CLAB, space-suit CVC placement, and DVT prophylaxis, the infection & DVT rates might be less of a problem.

But the placement issues -- bleeding, neck hematoma, RP hemorrhage, pseudoaneurysm, fistula, or just not being able to place the line -- do still exist.

Plus, IJs and femoral veins both collapse during most cases of hypotension, making blind placement even more difficult. In cardiac arrest, the femoral vein might have the pulse.

Further, once you get over the learning hump (maybe 5 lines in someone who is remotely savvy?) I think that it is easier AND faster to place the lines under US.

And lastly, Scott Weingart puts it very well today: people don't immediately die if I can't get the line in (unlike failed airways).

With central lines, the blind approach works very well most of the time. However, Marty Tobin put it very well:

But here's the rub. The challenge of clinical medicine is not about taking care of the great majority of patients who do well irrespective of the methods employed by their physicians. Instead, the goal is to take feasible steps that have a high likelihood of circumventing a catastrophe in a small number of instances....Taking simple steps to prevent infrequent occurrences that lead to a clinical catastrophe should dictate the practice of medicine, rather than employing approaches that are convenient to physicians and successful in most patients. (PulmCCM; emphasis mine)

Compare with DL vs VL. As I mentioned during the discussion, the key points are that DL skills are translatable to VL; VL is easily defeated by a speck of blood, vomit, or mucus; equipment issues (ie what happens when your Glidescope blades are all getting strerilized?); and I had one more that I don't recall now. VL will get us the view in a higher percentage of cases (although you may not always be able to deliver the tube) but DL isn't as far behind as landmark lines are behind US lines. The gap is very different.

And I agree that the combo VL/DL devices are very different than the angulated devices, and allow for training of both juniors and skill maintenance over time. During my chief year I think I used the CMAC on nearly every tube but never looked at the screen unless I ran into trouble***

Lastly, Minh made a great but ultimately flawed analogy that I cannot let stand:

Giving someone a Glidescope doesn't make them a great intubator; it's not like how giving someone a lightsaber makes them a Jedi. - MLC (paraphrased

While the lightsaber is the weapon of the Jedi, it is not the source of the Jedi's power. For whatever reason, some people are just force sensitive (to varying degrees) and may be trained to hone those skills. (I do not believe the prequels to be canonical so we can ignore the microbiologic explanation of force sensitivity.)

Giving a monkey a McGRATH MAC doesn't make him an anesthesiologist, just as Luke didn't become a Jedi the moment Obi-Wan handed him his father's lightsaber.



*I do not want to simply explain myself out of some Jungian desire to resolve my cognitive dissonance (in fact, I don't even think Jung had anything to do with cognitive dissonance and simply used him here because he's the psychology giant whose name I know aside from Freud. Wikipedia states that Festinger coined the term) or some sort of unresolved father-issues. 

**both of them

***the jokes pretty much write themselves

This is adapted from an email I sent to Minh Le Cong.

Haney Mallemat recently hosted a number of us what will hopefully be the first in a long series of international EMCC real-time discussions, with participants including Haney, Scott Weingart, Rob Bryant, Jeremy Faust, Steve Caroll, myself, Laleh Gharahbaghian, and of course, the ubiquitous Minh Le Cong. (video of the discussion should hopefully be up at some point)

Two related topics came up:

1. Is DL dead? 
2. Is ultrasound necessary for IJ & femoral lines?

It is not lost on me that these are very similar questions, and I come down on different sides with each.* I want to explain why I see 2 very similar situations and come to 2 different conclusions.

With respect to ultrasound for IJ & femoral lines, I think that it is clear that the landmarks are simply not reliable. I don't have hard references (although people who taught me assure me they exist) but the Sinai US guru Bret Nelson loves to take junior residents, show them the nice "NAVEL" shot and then scan up and down and show how the anatomy changes -- the relationship between the femoral artery and vein is much more complex, variable, and dangerous. I have done this on nearly every femoral line I have done** and it is shocking. Similarly, Scott Weingart has shown data on the IJ similarly just not being reliably related to the carotid.

I think Marik is possibly (probably?) correct and in the era of monitoring CLAB, space-suit CVC placement, and DVT prophylaxis, the infection & DVT rates might be less of a problem.

But the placement issues -- bleeding, neck hematoma, RP hemorrhage, pseudoaneurysm, fistula, or just not being able to place the line -- do still exist.

Plus, IJs and femoral veins both collapse during most cases of hypotension, making blind placement even more difficult. In cardiac arrest, the femoral vein might have the pulse.

Further, once you get over the learning hump (maybe 5 lines in someone who is remotely savvy?) I think that it is easier AND faster to place the lines under US.

And lastly, Scott Weingart puts it very well today: people don't immediately die if I can't get the line in (unlike failed airways).

With central lines, the blind approach works very well most of the time. However, Marty Tobin put it very well:

But here's the rub. The challenge of clinical medicine is not about taking care of the great majority of patients who do well irrespective of the methods employed by their physicians. Instead, the goal is to take feasible steps that have a high likelihood of circumventing a catastrophe in a small number of instances....Taking simple steps to prevent infrequent occurrences that lead to a clinical catastrophe should dictate the practice of medicine, rather than employing approaches that are convenient to physicians and successful in most patients. (PulmCCM; emphasis mine)

Compare with DL vs VL. As I mentioned during the discussion, the key points are that DL skills are translatable to VL; VL is easily defeated by a speck of blood, vomit, or mucus; equipment issues (ie what happens when your Glidescope blades are all getting strerilized?); and I had one more that I don't recall now. VL will get us the view in a higher percentage of cases (although you may not always be able to deliver the tube) but DL isn't as far behind as landmark lines are behind US lines. The gap is very different.

And I agree that the combo VL/DL devices are very different than the angulated devices, and allow for training of both juniors and skill maintenance over time. During my chief year I think I used the CMAC on nearly every tube but never looked at the screen unless I ran into trouble***

Lastly, Minh made a great but ultimately flawed analogy that I cannot let stand:

Giving someone a Glidescope doesn't make them a great intubator; it's not like how giving someone a lightsaber makes them a Jedi. - MLC (paraphrased

While the lightsaber is the weapon of the Jedi, it is not the source of the Jedi's power. For whatever reason, some people are just force sensitive (to varying degrees) and may be trained to hone those skills. (I do not believe the prequels to be canonical so we can ignore the microbiologic explanation of force sensitivity.)

Giving a monkey a McGRATH MAC doesn't make him an anesthesiologist, just as Luke didn't become a Jedi the moment Obi-Wan handed him his father's lightsaber.



*I do not want to simply explain myself out of some Jungian desire to resolve my cognitive dissonance (in fact, I don't even think Jung had anything to do with cognitive dissonance and simply used him here because he's the psychology giant whose name I know aside from Freud. Wikipedia states that Festinger coined the term) or some sort of unresolved father-issues. 

**both of them

***the jokes pretty much write themselves